Evaluation of fetal absorbed doses from computed tomography examinations of pregnant patients: A systematic review

BACKGROUND: Currently, no systematic data are available on fetal radiation exposure as a result of radiographic studies during pregnancy. Consequently, there are no approved methods of its calculation that can be used in clinical practice. It is especially relevant for computed tomography scans as it is a widely used and highly informative method of diagnostic imaging associated with high exposure levels. AIM: to systematize currently available data on radiation dose absorbed by the fetus from computed tomography scans in pregnant women. MATERIALS AND METHODS: The search for publications in Russian and English was conducted in PubMed/Medline, Google Scholar and еLibrary. The final analysis included 12 papers including 8 studies using human body phantoms, 3 retrospective studies and one prospective clinical study. RESULTS: Abdominal and pelvic computed tomography scans as well as whole-body scans were found to be associated with the highest fetal radiation exposure. However, in none of the publications the fetal exposure limit was exceeded. CONCLUSION: Clinically indicated non-contrast-enhanced computed tomography scans in pregnant women are not likely to be associated with the fetal absorbed doses that exceed the limit of 100 mGy regardless of the scanned area. However, this limit might be exceeded in case of performing multiple studies or if multiphase abdominal or pelvic computed tomography scans, or whole-body computed tomography scans are performed in patients with multiple trauma. In these cases, a decision regarding the need for these investigations should be made by a multi-disciplinary team (including radiation safety specialists, diagnostic radiologists and clinicians) based on the results of additional risk assessment

Extracellular nucleotide regulation and signaling in cardiac fibrosis.

Following myocardial infarction, purinergic nucleotides and nucleosides are released via non-specific and specific mechanisms in response to cellular activation, stress, or injury. These extracellular nucleotides are potent mediators of physiologic and pathologic responses, contributing to the inflammatory and fibrotic milieu within the injured myocardium. Via autocrine or paracrine signaling, cell-specific effects occur through differentially expressed purinergic receptors of the P2X, P2Y, and P1 families. Nucleotide activation of the ionotropic (ligand-gated) purine receptors (P2X) and several of the metabotropic (G-protein-coupled) purine receptors (P2Y) or adenosine activation of the P1 receptors can have profound effects on inflammatory cell function, fibroblast function, and cardiomyocyte function. Extracellular nucleotidases that hydrolyze released nucleotides regulate the magnitude and duration of purinergic signaling. While there are numerous studies on the role of the purinergic signaling pathway in cardiovascular disease, the extent to which the purinergic signaling pathway modulates cardiac fibrosis is incompletely understood. Here we provide an overview of the current understanding of how the purinergic signaling pathway modulates cardiac fibroblast function and myocardial fibrosis

Host A2B Adenosine Receptors Promote Carcinoma Growth1

Recent studies suggest that tumor-infiltrating immune cells can benefit the tumor by producing factors that promote angiogenesis and suppress immunity. Because the tumor microenvironment is characterized by high adenosine levels, we hypothesized that the low-affinity A2B adenosine receptor located on host immune cells may participate in these effects. In the current study, we tested this hypothesis in a Lewis lung carcinoma isograft model using A2B receptor knockout (A2BKO) mice. These mice exhibited significantly attenuated tumor growth and longer survival times after inoculation with Lewis lung carcinoma compared to wild type (WT) controls. Lewis lung carcinoma tumors in A2BKO mice contained significantly lower levels of vascular endothelial growth factor (VEGF) compared to tumors growing in WT animals. This difference was due to VEGF production by host cells, which comprised 30 ± 2% of total tumor cell population. Stimulation of adenosine receptors on WT tumor-infiltrating CD45+ immune cells increased VEGF production fivefold, an effect not seen in tumor-associated CD45+ immune cells lacking A2B receptors. In contrast, we found no significant difference in VEGF production between CD45- tumor cells isolated from WT and A2BKO mice. Thus, our data suggest that tumor cells promote their growth by exploiting A2B adenosine receptor-dependent regulation of VEGF in host immune cells